The proposal is to identify brain, behavioral, and self-report predictors of progression to changes in smoking rate and nicotine dependence in 128 young light smokers (YLS) in a longitudinal design using a number of novel predictors, including individual differences (IDs) in EEG and reward sensitivity at baseline and in response to standardized and to self-selected acute nicotine doses (ANIC). The associations of a compelling genetic functional variant polymorphism, rs16969968, in the alpha5 nicotinic receptor subunit will also be related to smoking progression and ANIC responses. The predictors will be attentional, affective, and reward-related processes assessed with brain (electrocortical), behavioral, and self-report indices that are well validated as responsive to ANIC in nicotine-dependent (ND) smokers. Evidence indicates that initial responses to first smoking experience, progression from light to regular smoking, and progression to ND are influenced by both genetic and environmental factors. There is good reason to hypothesize that better characterization of IDs in the effects of ANIC on attention, mood, and brain reactivity in YLS will provide important insights into mechanisms that contribute to the reinforcement of smoking and smoking trajectories in YLS. Such information could lead to targeted pharmacotherapy and behavioral interventions for at-risk YLS. The following hypotheses would be tested in a population of YLS: 1) ANIC will increase attention performance, mood, and resistance distraction by emotionally negatively valent pictures and words and that these beneficial (reinforcing) effects will predict changes in smoking rate 3, 6, 12, and 18 months later, 2) Lower baseline attentional and emotional levels will predict greater increases in smoking at the follow-ups. 3) Electrocortical (EEG, ERP, and source localization analyses) indices of low EEG activity (high theta & alpha power), reduced P3b amplitude, and greater reductions in P3b to targets following negatively valent distractor will predict increased smoking during nicotine deprived states and 4) hypotheses 1-3 will be supported even after controlling for social factors that may promote change in smoking. Secondary exploratory analyses will include the relationships of the functional variant polymorphism rs16969968 of the alpha5-alpha3-beta4 nicotinic receptor gene cluster to changes in smoking and to other predictors of change, including responses to ANIC.